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Brad Fortune, Marcus A. Bearse, George A. Cioffi, Chris A. Johnson; Selective Loss of an Oscillatory Component from Temporal Retinal Multifocal ERG Responses in Glaucoma. Invest. Ophthalmol. Vis. Sci. 2002;43(8):2638-2647.
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purpose. To evaluate electrophysiologic function in glaucoma by using a new stimulus designed to enhance ganglion cell and optic nerve head component (ONHC) contributions to multifocal electroretinogram (mfERG) responses.
methods. mfERGs of 16 individuals with glaucoma (POAG) and 18 normal control subjects were recorded and analyzed with a VER imaging system. The stimulus had three frames inserted between each m-sequence step: a full-field dark frame (1.0 cd/m2), a full-field flash (200 cd/m2), and another dark frame. Multifocal flashes were 100 cd/m2. The stimulus subtended approximately 40° total diameter and contained 103 scaled hexagonal elements. Signals were obtained using Burian-Allen bipolar electrodes, amplified ×106, band-pass filtered at 10 to 300 Hz, and sampled at 1200 Hz.
results. Local first-order responses (kernels) consisted of a direct component (DC) followed by an induced component (IC). Nasal–temporal response asymmetries in normal eyes were most easily observed in the IC. A small but distinct oscillation in the ICs of temporal retinal responses distinguished them from nasal IC waveforms. In individuals with glaucoma, there was less asymmetry between nasal and temporal responses, mostly because of the reduction of the oscillation in the temporal retinal ICs. The amplitude of this oscillation was 4.4 ± 2.1 nV/deg2 in the control group and 1.8 ± 1.2 nV/deg2 in the glaucoma group (P < 0.0001). Amplitude and latency measures of other response features were not significantly different from normal. Amplitude of the IC oscillation was not correlated with age in either the normal or glaucoma groups. In a group of normal subjects retested 3 months later, the average test–retest repeatability was ±12%.
conclusions. Selective loss of an oscillatory feature from IC responses in glaucoma may represent abnormalities in the inner plexiform layer of the temporal retina, where classic oscillatory potentials (OPs) are thought to arise. However, evidence suggests that this effect may also be due in part to loss of the ONHC.
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